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Copyright 2005, American Phytopathological Society. Used by permission.

Abstract

Seed contamination with polyketide mycotoxins, including aflatoxin (AF) and sterigmatocystin (ST) produced by Aspergillus spp., is an agricultural, economic, and medical issue worldwide. Acetyl-CoA, the fundamental building block of all known fungal polyketides, is generated by a large number of biochemical pathways, including β-oxidation of fatty acids and glycolysis of sugars. We present several lines of evidence to support a major role for seed fatty acids in formation of AF and ST in A. flavus, A. parasiticus, and A. nidulans. Aspergillus strains exhibiting canonical signs of oleic acid–induced peroxisome proliferation, including increased catalase activity, β-oxidation gene expression, and peroxisomal clustering, also exhibited a marked increase in toxin gene expression and biosynthesis. Furthermore, microscopic observations showed that the ST and AF precursor norsolorinic acid accumulated in peroxisomes of all three Aspergilli. While a peroxisomal β-oxidation mutation eliminated oleic acid–induced increases in ST in A. nidulans, a mitochondrial β-oxidation mutation played a larger role in eliminating ST formation on oatmeal medium and on live corn kernels, implicating a fundamental role for both peroxisomal and mitochondrial β-oxidation in toxin production.